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Stretch activation is defined as a delayed increase in force after rapid stretches. Although there is considerable evidence for stretch activation in isolated cardiac myofibrillar preparations, few studies have measured mechanisms of stretch activation in mammalian skeletal muscle fibers. We measured stretch activation following rapid step stretches [∼1%–4% sarcomere length (SL)] during submaximal Ca2+ activations of rat permeabilized slow-twitch skeletal muscle fibers before and after protein kinase A (PKA), which phosphorylates slow myosin binding protein-C. PKA significantly increased stretch activation during low (∼25%) Ca2+ activation and accelerated rates of delayed force development ( kef) during both low and half-maximal Ca2+ activation. Following the step stretches and subsequent force development, fibers were rapidly shortened to original sarcomere length, which often elicited a shortening-induced transient force overshoot. After PKA, step shortening-induced transient force overshoot increased ∼10-fold following an ∼4% SL shortening during low Ca2+ activation levels. kdf following step shortening also increased after PKA during low and half-maximal Ca2+ activations. We next investigated thin filament regulation of stretch activation. We tested the interplay between cardiac troponin I (cTnI) phosphorylation at the canonical PKA and novel tyrosine kinase sites on stretch activation. Native slow-skeletal Tn complexes were exchanged with recombinant human cTn complex with different human cTnI N-terminal pseudo-phosphorylation molecules: 1) nonphosphorylated wild type (WT), 2) the canonical S22/23D PKA sites, 3) the tyrosine kinase Y26E site, and 4) the combinatorial S22/23D + Y26E cTnI. All three pseudo-phosphorylated cTnIs elicited greater stretch activation than WT. Following stretch activation, a new, elevated stretch-induced steady-state force was reached with pseudo-phosphorylated cTnI. Combinatorial S22/23D + Y26E pseudo-phosphorylated cTnI increased kdf. These results suggest that slow-skeletal myosin binding protein-C (sMyBP-C) phosphorylation modulates stretch activation by a combination of cross-bridge recruitment and faster cycling kinetics, whereas cTnI phosphorylation regulates stretch activation by both redundant and synergistic mechanisms; and, taken together, these sarcomere phosphoproteins offer precision targets for enhanced contractility.

ImportanceSex-specific differences in the commonly used cardiac biomarkers high-sensitivity cardiac troponin (hs-cTn) and N-terminal pro–brain natriuretic peptide (NT-proBNP) are apparent. There is an absence of medical literature delineating the concentration differences for these biomarkers in transgender individuals without cardiac disease.ObjectiveTo determine the distribution of hs-cTn and NT-proBNP in healthy transgender people.Design, Setting, and ParticipantsIn this cross-sectional prospective study, healthy transgender individuals prescribed testosterone or estradiol for 12 months or more were recruited from internal medicine and primary care clinics that specialize in transgender medical care between November 1, 2017, and July 1, 2018.ExposuresTestosterone or estradiol for 12 months.Main Outcomes and MeasuresConcentrations for hs-cTnI (troponin I), hs-cTnT (troponin T), and NT-proBNP were measured.ResultsTransgender people prescribed testosterone (n = 79; mean [SD] age, 28.8 [7.8] years) or estrogen (n = 93; mean [SD] age, 35.1 [11.7] years) were recruited. The concentration of hs-cTn was significantly higher in transgender men relative to transgender women. For Abbott hs-cTnI levels, the median (IQR) concentration observed in transgender men and women was 0.9 (0.6-1.7) ng/L and 0.6 (0.3-1.0) ng/L, respectively. Results were similar across 2 additional hs-cTn assays. In contrast, NT-proBNP level was higher in transgender women. The median (IQR) NT-proBNP concentration was significantly higher in transgender women ( 49 [32-86] ng/L) than in transgender men (17 [13-27] ng/L).Conclusions and RelevanceFindings of this cross-sectional study suggest that the differences in concentration for hs-cTn and NT-proBNP between transgender men and women were similar to what is observed between cisgender men and women. Sex hormones, rather than sex assigned at birth, may be a stronger driver of the observed concentration differences between healthy men and women for biomarkers of cardiac disease.

SUMMARY OBJECTIVE: A reliable predictor is needed for non-ST-elevation myocardial infarction patients with high mortality risk. The aim of this study was to assess the effectiveness of the Global Registry of Acute Coronary Events and Quick Sequential Organ Failure Assessment-Troponin (qSOFA-T) scores on in-hospital mortality rate in non-ST-elevation myocardial infarction patients. METHODS: This is an observational and retrospective study. Patients admitted to the emergency department with acute coronary syndrome were evaluated consecutively. A total of 914 patients with non-ST-elevation myocardial infarction who met inclusion criteria were included in the study. The Global Registry of Acute Coronary Events and qSOFA scores were calculated and investigated its contribution to prognostic accuracy by adding cardiac troponin I (cTnI) concentration to the qSOFA score. The threshold value of the investigated prognostic markers was calculated by receiver operating characteristic curve analysis. RESULTS: We found the in-hospital mortality rate to be 3.4%. The area under the receiver operating characteristic curve for Global Registry of Acute Coronary Events and qSOFA-T is 0.840 and 0.826, respectively. CONCLUSION: The qSOFA-T score, which can be calculated easily, quickly, and inexpensively and obtained by adding the cTnI level, had excellent discriminatory power for predicting in-hospital mortality. Difficulty in calculating the Global Registry of Acute Coronary Events score, which requires a computer, can be considered a limitation of this method. Thus, patients with a high qSOFA-T score are at an increased risk of short-term mortality.

Background: To examine the association of ultrasensitive cTnI (cardiac troponin I) with incident cardiovascular disease events (CVDs) in the primary prevention setting. Methods: cTnI was analyzed in the baseline plasma (2008–2012) of CVD-free volunteers from the Paris Prospective Study III using a novel ultrasensitive immunoassay (Simoa Troponin-I 2.0 Kit, Quanterix, Lexington) with a limit of detection of 0.013 pg/mL. Incident CVD hospitalizations (coronary heart disease, stroke, cardiac arrhythmias, deep venous thrombosis or pulmonary embolism, heart failure, or arterial aneurysm) were validated by critical review of the hospital records. Hazard ratios were estimated per log-transformed SD increase of cTnI in Cox models using age as the time scale. Results: The study population includes 9503 participants (40% women) aged 59.6 (6.3) years. cTnI was detected in 99.6% of the participants (median value=0.63 pg/mL, interquartile range, 0.39–1.09). After a median follow-up of 8.34 years (interquartile range, 8.0–10.07), 516 participants suffered 612 events. In fully adjusted analysis, higher cTnI (per 1 SD increase of log cTnI) was significantly associated with CVD events combined (hazard ratio, 1.18 [1.08–1.30]). Among all single risk factors, cTnI had the highest discrimination capacity for incident CVD events (C index=0.6349). Adding log cTnI to the SCORE 2 (Systematic Coronary Risk Evaluation) risk improved moderately discriminatory capacity (C index 0.698 versus 0.685; bootstrapped C index difference: 0.0135 [95% CI, 0.0131–0.0138]), and reclassification of the participants (categorical net reclassification index, 0.0628 [95% CI, 0.023–0.102]). Findings were consistent using the US pooled cohort risk equation. Conclusions: Ultrasensitive cTnI is an independent marker of CVD events in the primary prevention setting.

In the past studies, it is shown that cardiac troponin I (cTnI, encoded by TNNI3), as a cytoplasmic protein, is an inhibitory subunit in troponin complex, and involves in cardiomyocyte diastolic regulation. Here, we assessed a novel role of cTnI as a nucleoprotein. Firstly, the nuclear translocation of cTnI was found in mouse, human fetuses and rat heart tissues. In addition, there were differences in percentage of intranuclear cTnI in different conditions. Based on weighted gene co-expression network analyses (WGCNA) and verification in cell experiments, a strong expression correlation was found between TNNI3 and Atp2a2, which encodes sarco-endoplasmic reticulum Ca2+ ATPase isoform 2a (SERCA2a), and involves in ATP hydrolysis and Ca 2+ transient. TNNI3 gain and loss caused Atpa2a2 increase/decrease in a dose-dependent manner both in mRNA and protein levels, in vivo and in vitro. By using ChIP-sequence we demonstrated specific binding DNA sequences of cTnI were enriched in ATP2a2 promoter −239∼-889 region and the specific binding sequence motif of cTnI was analyzed by software as "CCAT", which has been reported to be required for YY1 binding to the promoter region of YY1-related genes. Moreover, it was further verified that pcDNA3.1 (−)-TNNI3 could express cTnI proteins and increase the promoter activity of Atp2a2 through luciferase report assay. In the end, we evaluated beat frequencies, total ATP contents, Ca 2+ transients in TNNI3-siRNA myocardial cells. These findings indicated, for the first time, cTnI may regulate Atp2a2 in cardiomyocytes as a co-regulatory factor and participate in the regulation of intracellular Ca ions.

Coronavirus disease 2019 (COVID-19) was declared a pandemic and has spread around the globe, unsparingly affecting vulnerable populations. Effective prevention measures for pregnant women, who are particularly affected, include early identification of those patients at risk of developing in-hospital complications, and the continuous improvement of maternal-fetal treatment strategies to ensure the efficient use of health resources. The objective of our retrospective study was to determine which patient biomarkers on hospital admission correlate with disease severity as measured by disease course classification, the need for oxygen supplementation and higher demand for oxygen, the need for mechanical ventilation, intensive care unit admission, and length of hospital stay. Analysis of 52 PCR SARS-CoV-2 positive pregnant women revealed that the median date of hospital admission was the 30th gestational week, with dyspnoea, cough, and fever as the leading symptoms. The presence of diabetes and hypertension predisposed pregnant women to the severe course of illness. Lung involvement shown by CT scans on admission correlated with the greater clinical severity. The main laboratory predictors of disease progression were lymphocytopenia, hypocalcemia, low total cholesterol, low total protein levels, and high serum levels of C-reactive protein, ferritin, interleukin-6, glucose, lactate dehydrogenase, procalcitonin, and troponin I. Further research with a larger cohort of pregnant women is needed to determine the utility of these results for everyday practice.

Herein, an exogenous luminophore-free and disposable electrochemiluminescence (ECL) biosensor was established for rapid response of acute myocardial infarction (AMI) using programmable Y-shaped probes (Y-probes) with proximity bivalent recognition. Specifically, the indium tin oxide thin film coated glass electrode (ITO) was modified with urchin-like porous TiO

Pulmonary embolism (PE) often occurs secondary to deep vein thrombosis and is an important cause of mortality and morbidity. This study aimed to evaluate the relationship between YKL-40 level and clinical risk score in patients with PE.The study included a total of 100 patients, 80 patients diagnosed with PE in the emergency department and 20 healthy controls. Patients with PE were divided into four groups: high-risk patients (n = 20), high-intermediate-risk patients (n = 20), low-intermediate-risk patients (n = 20), and low-risk patients (n = 20). Serum YKL-40 levels were measured by enzyme-linked immunosorbent assay. Pulmonary artery obstruction index (PAOI) was calculated from computed tomography angiography images.PAOI increased in correlation with PE risk and differed significantly between all patient groups (p 0.001). Troponin-I levels were significantly higher in the high-risk and high-intermediate-risk groups compared to the other groups (p 0.001), but did not differ significantly between high-risk and high-intermediate-risk patients (p = 0.09). YKL-40 level was significantly higher in the high-risk PE group than the high-intermediate-risk group (p 0.001). In receiving operator characteristic curve analysis assessing the discriminatory value of YKL-40 for high-risk PE patients, a cut-off value of 227.2 ng/mL had sensitivity of 85 % and specificity of 70 %.YKL-40 may be an important biomarker in decisions regarding early thrombolytic treatment in patients with high-intermediate-risk PE. In addition, medical treatments targeting YKL-40 may also reduce thrombotic tendency in high-risk patient groups.

Melatonin has emerged as an anti-inflammatory agent, potent direct free-radical scavenger, and an indirect antioxidant in preventing ischemia-reperfusion injury. This study aimed to evaluate melatonin's effect on cardiac biomarkers after coronary artery bypass grafting (CABG).A double-blind, randomized placebo-controlled pilot clinical study.Booali Sina Hospital, Qazvin University of Medical Sciences, Qazvin, Iran.One hundred patients undergoing elective CABG. The patients were divided randomly into control (C) and melatonin (M) groups (50 patients per group).The M group received 3 mg of melatonin the night before surgery, 3 mg in the morning, and routine cardiac surgery medications. The C group received 1 placebo tablet rather than melatonin. After surgery, the patients in the M group received 3 mg of melatonin, and the C group received 1 placebo tablet at bedtime until the third day after CABG.In both groups, creatine kinase-MB (CPK-MB), cardiac troponin I, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) were measured before surgery and on the first, second, and third postoperative days. Serum CPK-MB levels on the second and third day after CABG were significantly lower in the M group than in the C group (p0.05). Regarding cardiac troponin I, CRP, and ESR markers, there were no significant changes in serum concentration before surgery and on the first, second, and third days after surgery between the 2 groups (p0.05). The mean length of hospitalization in the ICU was lower in the M group (3.4 ± 1.05) compared with the C group (3.96 ± 1.06, p = 0.01).Melatonin reduced the postoperative level of CPK-MB and the length of hospitalization in the ICU in patients who underwent cardiac surgery.

We examined the safety and efficacy of del Nido cardioplegic solution compared with histidine-tryptophan-ketoglutarate cardioplegic solution in minimally invasive cardiac surgery.Patients who underwent minimally invasive cardiac surgery using del Nido or histidine-tryptophan-ketoglutarate from 2015 to 2019 were enrolled. Various clinical outcomes were compared between the groups. Postoperative laboratory findings including the levels of electrolytes, cardiac enzymes (creatine kinase-MB and troponin I), and serial blood lactate were also measured and compared. Based on 28 baseline covariates, propensity score matching was performed to reduce selection bias.Among 766 patients, del Nido and histidine-tryptophan-ketoglutarate were used in 330 patients (43.1%) and 436 patients (56.9%), respectively. There were no significant intergroup differences in postoperative clinical outcomes and early adverse outcomes among 228 pairs of propensity score-matched patients. Immediate postoperative sodium levels were within the normal range in both groups without a significant difference (P = .50). However, peak creatine kinase-MB (median, 31.9 vs 37.7 ng/mL, P = .026) and troponin I (6.9 vs 9.1 ng/mL, P = .014) levels were significantly lower in the del Nido group. Linear regression analysis revealed a significant association between the peak cardiac enzyme levels and the cardiac ischemic time depending on the cardioplegia type, with lower cardiac isoenzymes for del Nido over histidine-tryptophan-ketoglutarate (P .001) until the crossover point at the cardiac ischemic time over 100 minutes.In comparison with histidine-tryptophan-ketoglutarate solution, del Nido solution seems to have acceptable safety and efficacy with good myocardial protection in minimally invasive cardiac surgery. Further studies focusing on complex surgeries requiring longer cardiac ischemic time are needed.

To compare the effects of dexmedetomidine (DEX) pretreatment, posttreatment, and whole-course pumping on myocardial protection during cardiac valve replacement.One hundred and twenty patients undergoing cardiac valve replacement were randomly divided into the follow groups: DEX pretreatment (D1 group), DEX posttreatment (D2 group), DEX whole-course pumping (D3 group), and Control (C group). The concentrations of cardiac troponin I (cTnI), malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), rate of spontaneous heart rebound after aortic opening, time to heart rebound, incidence of arrhythmia, and use of sufentanil and vasoactive drugs were recorded.Compared with group C, the concentrations of cTnI, MDA, and TNF-α in the D1, D2, and D3 groups were lower, especially in the latter. The time to heart rebound was prolonged in all three groups (P0.05). The rate of automatic rebound was increased (P0.05) while the incidence of arrhythmia was decreased (P0.05) in all groups compared with group C. Group D3 had the highest rate of automatic rebound and the lowest incidence of arrhythmia. Compared with groups C and D2, the use of sufentanil and dopamine was lower in groups D1 and D3 (P0.05), especially in the latter.During cardiac valve replacement, DEX pretreatment, posttreatment, and whole-course pumping could have myocardial protective effects. The latter showed better effects.

Recently emerged Z-scheme heterostructure-based immunoassays have presented new opportunities for photoelectrochemical (PEC) biosensing development. Here, we described a tunable signal-on PEC biosensor for the detection of cardiac troponin I (cTnI), which exploited a competitive absorption effect between Cu(II) ions and a Zr metal-organic framework (Zr-MOF) constructed on TiO

Owing to its simplicity, high throughput, and ultrasensitivity, single-particle collision electrochemistry (SPCE) has attracted great attention in biosensing, especially labeled SPCE. However, the low signal conversion efficiency and much interference from complex samples limit its wide application. Here, a new and robust SPCE immunosensor was proposed for ultrasensitive cardiac troponin I (cTnI) detection by combining target-driven rolling circle amplification (RCA) with magnetic beads (MBs). Antibody-modified MBs have good stability, dispersity, and magnetic response capacity in complex samples, enabling efficient capture and separation of cTnI with high specificity and anti-interference ability. The presence of cTnI could specifically drive the formation of magnetic immunocomplexes followed by triggering RCA and enzyme digestion reaction. By using Pt nanoparticles (Pt NPs)-modified ssDNA as signal probes, one cTnI molecule could induce the release of 4.5 × 10

Several studies have demonstrated an association between elevated cardiac biomarkers and adverse outcomes in patients with COVID-19. However, the prognostic and predictive capability of a multimarker panel in a prospectively collected, diverse "all-comers" COVID-19 population has not been fully elucidated.We prospectively assessed high sensitivity cardiac troponin I (hsTnI), NT-pro B-type Natriuretic Peptide (NT-proBNP), Galectin-3 (Gal-3), and procalcitonin (PCT) in 4,282 serial samples from 358 patients admitted with symptomatic, RT-PCR confirmed SARS-CoV-2 infection. Outcomes examined were 30-day in-hospital mortality and requirement for intubation within 10 days.Baseline hsTnI had the highest AUC for predicting 30-day mortality (0.81; 95% CI, 0.73-0.88), followed by NT-proBNP (0.80; 0.74-0.86), PCT (0.77; 0.70-0.84), and Gal-3 (0.68; 0.60-0.76). HsTnI 3.5 ng/L at baseline identified patients at low risk for in-hospital mortality (NPV 95.9%, sensitivity 97.3%) and 10-day intubation (NPV 90.4%, sensitivity 88.5%). Continuous, log-2 increases in troponin concentration were associated with reduced survival (p 0.001) on Kaplan-Meier curves and increased risk of 30-day mortality: HR 1.26 (1.16-1.37) in univariate and 1.19 (1.03-1.4) in multivariate models. Time-varying doubling of concentrations of hsTnI and Gal-3 were associated with increased risk of 30-day mortality (adjusted HR 1.21, 1.06-1.4, and 1.92, 1.40-2.6).HsTnI, NT-proBNP, Gal-3, and PCT are elevated at baseline in patients that have worse outcomes from COVID-19. HsTnI was the only independent predictor of 30-day mortality and intubation. Time-varying, doubling in hsTnI and Gal-3 further aided in prognostication of adverse outcomes. These results support the use of hsTnI for triaging patients with COVID-19.

Early diagnosis of coronary artery disease (CAD) in patients with chest pain is a challenge. Currently diagnosis of CAD is confirmed by coronary angiography, which is invasive and not easily available in developing countries. Therefore, it is imperative to establish noninvasive biomarker for early diagnosis of CAD in patients with angina and determine the diagnostic accuracy of inflammatory biomarkers of atherosclerosis in comparison to angiography and correlate with severity of CAD in patients with angina. Diagnostic accuracy study was carried out in tertiary care hospitals, Rawalpindi, Pakistan. Total of 58 patients aged 55.24 ± 11.61 years, with chest pain and troponin-I -ve, having coronary artery stenosis ≥50% were included as cases of CAD and 55 subjects having stenosis50% were included as controls. Nuclear factor kappa-B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hs-CRP) were analyzed on immunoassay analyzers. The receiver operating characteristic curve analysis revealed significant (

To examine the effect of Shenmai Injection (SMJ) on ferroptosis during myocardial ischemia reperfusion (I/R) injury in rats and the underlying mechanism.A total of 120 SPF-grade adult male SD rats, weighing 220-250 g were randomly divided into different groups according to a random number table. Myocardial I/R model was established by occluding the left anterior descending artery for 30 min followed by 120 min of reperfusion. SMJ was injected intraperitoneally at the onset of 120 min of reperfusion, and erastin (an agonist of ferroptosis), ferrostatin-1 (Fer-1, an inhibitor of ferroptosis) and ML385 (an inhibitor of nuclear factor erythroid-2 related factor 2 (Nrf2)) were administered intraperitoneally separately 30 min before myocardial ischemia as different pretreatments. Cardiac function before ischemia, after ischemia and after reperfusion was analysed. Pathological changes in the myocardium and the ultrastructure of cardiomyocytes were observed, and the myocardial infarction area was measured. Additionally, the concentration of FeCompared with the sham group, I/R significantly injured heart tissues, as evidenced by the disordered, ruptured and oedematous myocardial fibres; the increases in infarct size, serum CK-MB, cTnI and MDA levels, and myocardial FeFerroptosis is involved in myocardial I/R injury. Pretreatment with SMJ alleviated myocardial I/R injury by activating Nrf2/GPX4 signalling-mediated ferroptosis, thereby providing a strategy for the prevention and treatment of ischemic heart diseases.

Adipose-derived mesenchymal stem cells (Ad-MSCs) are promising candidates for cardiac repair/regeneration. The application of copolymer nanoscaffolds has received great attention in tissue engineering to support differentiation and functional tissue organization toward effective tissue regeneration. The objective of the current study was to develop functional and bioactive scaffolds by combining polycaprolactone (PCL) and polylactic acid (PLA) for cardiomyocyte differentiation of human Ad-MSC (hAd-MSCs) in the absence or presence of 5-azacytidine and transforming growth factor-β (TGF-β). To that end, the human MSCs were extracted from human adipose tissue (AD). The cardiomyocyte differentiation potency of hAd-MSCs was evaluated on the novel synthetic PCL/PLA nanofiber scaffolds prepared in the absence and presence of 5-azacytidine and TGF-β supplements. A PCL/PLA nanofibrous scaffold was fabricated using the electrospinning method and its nanotopography and porous structure were characterized using scanning electron microscopy. In addition, the attachment of hAd-MSCs on the PCL/PLA scaffolds was semiquantitatively investigated. Compared with other treatments, the PCL/PLA nanofibrous scaffold supplemented with both 5-azacytidine and TGF-β was observed to differentiate hAd-MSCs into cardiomyocytes at Day 21 as evidenced by real-time PCR for cardiac-specific genes including cardiac troponin I (cTnI), GATA4, MYH7, and NKX2.5. In addition, flow cytometric analysis of cTnI-positive cells demonstrated that the cardiomyocyte differentiation of hAd-MSCs was more efficient on the PCL/PLA nanofibrous scaffold supplemented with both 5-azacytidine and TGF-β than it was in the other treatment groups. Generally speaking, the results show that PCL/PLA nanofibrous scaffolds may be applied as a platform for efficient differentiation of hAd-MSCs into functional cardiomyocytes.

Electrocardiographically occult occlusive myocardial infarction (OOMI), defined as coronary artery occlusion requiring revascularization without ST-segment elevation on electrocardiogram (ECG), is associated with delayed diagnosis resulting in higher morbidity. Left ventricular (LV) wall motion abnormalities (WMA) appreciated on echocardiography can expedite OOMI diagnosis. We sought to determine whether point-of-care ultrasound (PoCUS) demonstrating WMA expedites revascularization time when performed on emergency department patients being evaluated for OOMI.This was a single-site retrospective cohort study over a 38-month period. All admitted adult ED patients ≥35 years of age evaluated by the emergency physician with PoCUS for LV function, an ECG, and a standard troponin I biomarker assay were included. Patients with ST-segment elevation myocardial infarction (STEMI), prior LV dysfunction, fever ≥100.4 °F, or hypotension were excluded. A structured chart abstraction was performed for relevant demographic and clinical characteristics.We screened 1561 ED patients who underwent cardiac PoCUS for eligibility: 874 met exclusion criteria, 453 were discharged, and 234 were included in the analysis. Twenty-three patients had coronary interventions, of which 14 had WMA. PoCUS was performed 36 min (IQR -9-68) before troponin resulted (n = 234) and 39 min (IQR -23-96) before the first troponin elevation (n = 85). Twenty of the 23 patients diagnosed with OOMI had elevated troponins prior to catheterization with time from PoCUS to first troponin elevation of 43 min (IQR 9-263). Of these patients, 11 had WMA identified on PoCUS, and the WMA was appreciated 47 min (IQR 26-255) prior to troponin elevation. The time from ED arrival to revascularization was 673 min (IQR 251-2158); 432 min (IQR 209-1300) among patients with WMA (n = 14) compared with 2158 min (IQR 552-3390) for those without WMA (n = 9).Cardiac PoCUS may identify OOMI earlier than standard evaluation and may expedite definitive management.

Objectives Postoperative cardiac troponin I concentration is predictive of worsened outcome in cardiac surgery. Lung transplantation (LT) surgery shares common features with cardiac surgery, but postoperative troponin has yet to be investigated. We aimed to evaluate the association between early postoperative troponin concentration and the 1-year mortality after transplantation. Design Retrospective, observational, single-centre study. Setting Tertiary care, university hospital. Participants Patients who underwent lung transplantation from January 2011 to December 2017 Interventions For each patient, preoperative, intraoperative, and postoperative data were collected, as well as the troponin I measurement at the moment of postoperative ICU admission. Measurements and Main Results Two hundred and twenty LT procedures were analysed. Troponin I was elevated in all LT patients with a median of 3.82 ng.ml−1 [2 - 6.42] ng.ml−1, being significantly higher in non-survivors than in survivors, 5.39 [2.88-7.44] versus 3.50 ng.ml−1 [1.74 - 5.76], p=0.005. In the multivariable analysis, we found that only the Simplified Acute Physiology Score II (SAPS 2) score (hazard ratio 1.03; 95% confidence interval [1.001; 1.05]; P=0.007) and the need to maintain extracorporeal life support (ECLS) at the end of surgery (hazard ratio 2.54; 95% confidence interval [1.36; 4.73]; p=0.003) were independently associated with the 1-year mortality. The multiple linear regression model found that troponin levels were associated with the need for ECLS (p=0.014), the amount of transfused packed red blood cells (PRBC) (p=0.008), and to the bilateral LT (p Conclusion Early postoperative troponin serum levels were not independently associated with 1-year mortality. Early postoperative troponin I levels were correlated to bilateral LT, need for ECLS, and intraoperative blood transfusion.

This randomized clinical trial was performed to compare pain scales between intravenous patient-controlled analgesia (IV-PCA) and patient-controlled epidural analgesia (PCEA) in patients undergoing open surgical resection of major pancreatobiliary malignancies.One hundred ten patients were randomly assigned to the PCEA or IV-PCA group. We compared the numeric rating scale pain score during ambulation on postoperative day (PD) 2 and at rest (at 06:00, 12:00, and 18:00) from PD 1 to 7, the serum level of troponin I on PD 1, and the incidence of postoperative complications between the two groups.There were no significant differences in the pain scores during ambulation on PD 2, at rest up to PD 7, serum troponin I level, and postoperative complication rates. The incidences of nausea (20.4% vs. 6.3%; p = 0.039) and drowsiness (20.4% vs. 0%; p = 0.001) were higher in the IV-PCA group and the rate of dysuria (0% vs. 14.6%; p = 0.004) was higher in the PCEA group.PCEA showed no superiority over IV-PCA in terms of postoperative pain relief or morbidity after major open surgery for pancreatobiliary malignancies. The method of analgesia should be considered based the characteristics of the patient, surgeon, anesthesiologist, and institute.

Plasma cell-free DNA (cfDNA) was elevated in patients with acute myocardial infarction (AMI) or heart failure (HF). However, whether cfDNA could serve as a predictor for risk of HF after AMI remains unknown. In this study, we conducted a pilot prospective cohort study in which 98 AMI patients were enrolled from a single center to assess the association between cfDNA levels at admission and risk of HF in an AMI population. Patients with cfDNA above the median level (14.39 ng/mL) showed higher low-density lipoprotein cholesterol, cardiac troponin I (cTnI), and soluble suppression of tumorigenicity 2 (sST2) levels compared with patients below the median. cfDNA was positively correlated with cTnI (

Aims To explore the association between elevated cardiac troponin I (cTnI) on 30-day mortality in patients with acute type A aortic dissection (ATAAD). Methods and results A total of 1321 consecutive patients who were admitted to the emergency department of Fuwai Hospital from January 2016 to December 2020 were enrolled. Patients had computed tomography-confirmed ATAAD and were measured serum cTnI on admission. Patients were divided into the troponin-positive (cTnI > 0.02 ng/mL) or the troponin-negative group (cTnI ≤ 0.02 ng/mL). Troponin was detected by PATHFAST instrument produced by Medins Co., Ltd., and the reference range of normal value is 0–0.02 ng/mL. A total of 522 out of 1321 patients (39.5%) in our study had elevated cTnI, who had higher 30–day mortality rate compared with the troponin-negative group (44.4% vs. 19.4% P < 0.0001). Multivariate logistic regression results showed that elevated cTnI was an independent risk indicator for 30-day mortality (odds ratio: 2.582; 95% confidence interval: 1.357–4.914; P = 0.0039). The addition of elevated cTnI level to a clinical-based risk prediction model resulted in significant incremental prognostic value (AUC difference: 0.0261). Conclusion Elevated cTnI is common in patients with ATAAD, and is associated with increased 30-day mortality risk.

Hemodialysis (HD) triggers recurrent and cumulative ischemic insults to the brain and the heart. Cooled dialysate may have a protective effect on major organs and improve hemodynamic tolerability of dialysis. The aim of the study was to compare HD with cooled dialysate with routine dialysis in terms of hemodynamic stability and levels of high-sensitivity Troponin I (hs-TnI) and N-terminal pro b-type natriuretic peptide (NTproBNP) pre and postdialysis.The 45 patients were randomized into two groups. The first group received a 35.5°C dialysate first (hypothermic dialysis) and the second group a 36.5°C dialysate first (routine dialysis). Then groups crossed over, so each group received the alternate dialysate (self-controls) For each patient, the first sample was collected at the beginning of dialysis, and a second sample was taken at the end of dialysis.hs-TnI and NTproBNP increased after routine HD by 10.7 ng\ml (p 0.001) and (12.0 pg/μl) (p 0.001), respectively, and by -3.1 ng\ml (p = 0.25) and (4.3 pg/μl) (p 0.001), respectively after hypothermic HD. Our study results showed a tendency towards less rise in hsTnI and NTproBNP during hypothermic HD (35.5°C) as compared to routine HD (36.5°C). Neither arm experienced statistically significant changes in blood pressure. Further studies in larger cohorts and long follow up are warranted in order to confirm that lower rise in (hs-TnI) and NTproBNP actually translate into lower clinical risk for cardiovascular events.

Evidence of the prognostic value of high-sensitivity troponin in patients with non-ischaemic heart failure (NIHF) is scarce. This study aimed to assess the predictive value of high-sensitivity cardiac troponin I (hs-cTnI) in NIHF patients.Hs-cTnI was measured at baseline in 650 NIHF patients admitted to the Heart Failure Center. The prognostic value of hs-cTnI was assessed based on a well-established model (including age, sex, New York Heart Association class, left ventricular ejection fraction, haemoglobin, sodium, estimated glomerular filtration rate, diabetes mellitus, treatment with angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, treatment with β-blockers, and NT-proBNP).During a median follow-up of 1036 days, 163 patients died of various causes. In total, 46.92% of patients had high hs-cTnI (hs-cTnI0.011 ng/ml). Over a 3-year follow-up, patients with high hs-cTnI (0.011 ng/ml) had a 1.54 [95% confidence interval (95% CI) 1.11-2.15] fold higher all-cause mortality risk than those without. Increasing concertation of hs-cTnI was also associated with a 23.0% (95% CI 13-33%, per logHs-cTnI provides significant prognostic value and could further remarkably improve risk stratification and prediction capabilities in NIHF patients.

This Research to Practice column assists to provide emergency advanced practice registered nurses an exploration of current evidence to establish implications for practice change within emergency care settings. The article, "Rapid Rule-Out of Myocardial Infarction After 30 Minutes as an Alternative to 1 Hour: The RACING-MI Cohort Study" by Bang et al. (2022), seeks to examine whether non-ST-segment elevation myocardial infarction identified on an electrocardiogram can be safely ruled out among a population of low-risk patients who present to the emergency department (ED) with undifferentiated acute chest pain. The study uses an accelerated 30-min testing algorithm of high-sensitivity troponin I markers as opposed to a traditional 1-hr high-sensitivity troponin I testing algorithm. The study results are presented to understand the factors of managing myocardial infarction (MI) and reducing patient length of stay surrounding MI care among ED providers at an emergency care center.

We evaluated the diagnostic performance of a whole blood, point of care (POC) high-sensitivity cardiac troponin I (hs-cTnI) assay for myocardial infarction (MI) compared to central laboratory assays.Consecutive patients presenting to the emergency department with symptoms of ischemia were studied. Serial hs-cTnI testing was based on clinical indication at presentation. Parallel measurements were made using fresh whole blood on Siemens Atellica VTLi POC assay, EDTA plasma on Abbott ARCHITECT i2000 used in practice, and heparin plasma on Siemens Atellica. MI was determined according to the Fourth Universal Definition of MI using 99th percentiles. Sensitivities and negative predictive values (NPV) were calculated using 99th percentile URLs.1089 Patients, 418 females and 671 males, were enrolled. There were 91 (8.4%) MIs. At baseline (0 h), POC hs-cTnI assay had a sensitivity of 65.7% (95% CI 47.8-80.9) for females and 67.9% (54.0-79.7) for males and NPV of 96.4% (93.9-98.1) for females and 96.7% (94.9-98.0) for males. At 2 h, sensitivity improved to 82.9% (66.4-93.4) for females and 80.4% (67.6-89.8) for males, while NPV improved to 98.2% (96.1-99.3) and 97.9% (96.3-99.0), respectively. For central laboratory assays, comparable diagnostics were observed at 2 h: females - sensitivity 94.3% (80.8-99.3) for ARCHITECT and 79.4% (62.1-91.3) for Atellica, and NPV 99.3% (97.6-99.9) and 98.0% (95.8-99.2), respectively; males - sensitivity 87.5% (75.9-94.8) for ARCHITECT and 80.4% (67.6-89.8) for Atellica, NPVs of 98.7% (97.3-99.5) and 97.9% (96.3-99.0), respectively.The POC, whole blood Atellica VTLi hs-cTnI assay demonstrated comparable diagnostic accuracy for MI to central laboratory assays using 99th percentiles.

The troponin core is an important regulatory complex in cardiac sarcomeres. Contraction is initiated by a calcium ion binding to cardiac troponin C (cTnC), initiating a conformational shift within the protein, altering its interactions with cardiac troponin I (cTnI). The change in cTnC–cTnI interactions prompts the C-terminal domain of cTnI to dissociate from actin, allowing tropomyosin to reveal myosin-binding sites on actin. Each of the concerted movements in the cardiac thin filament (CTF) is crucial for allowing the contraction of cardiomyocytes, yet little is known about the free energy associated with each transition, which is vital for understanding contraction on a molecular level. Using metadynamics, we calculated the free-energy surface of two transitions in the CTF: cTnC opening in the presence and absence of Ca(2+) and cTnI dissociating from actin with both open and closed cTnC. These results not only provide the free-energy surface of the transitions but will also be shown to determine if the order of transitions in the contraction cycle is important. From our calculations, we found that the calcium ion helps stabilize the open conformation of cTnC and that the C-terminus of cTnI is stabilized by cTnC in the open conformation when dissociating from the actin surface.

Troponin I levels are biomarkers of choice for diagnosis of acute myocardial infarction (AMI). However, prognostic significance of values below the 99th percentile upper reference limit (URL) in patients presenting with symptoms suggestive of Acute coronary syndrome (ACS) need further evaluation.The objectives of the study were to find the association of High sensitivity (hs)-Troponin I values below 99th percentile URL with age and the Emergency Department (ED) outcome, to determine single cut-off for safe discharge of these patients from the ED and to determine the 30-day outcome of the patients admitted under cardiac speciality.This is a retrospective study of patients presenting with suspicion of ACS in the ED between January 2019 till April 2021 and hs-Troponin I values below 99th percentile URL.Among 15,441 patients, 8034 (52%) were males and 7407 (48%) were females. 9677 (63%) of the patients had hs-Troponin I values5 ng/L while 5764 (37%) had values between 5 ng/L and 99th percentile URL. Higher hs-Troponin I values were associated with a worse ED outcome. Serial troponin I levels were performed in only 2.4% of the cohort. Receiver operating characteristics for ACS demonstrated an AUC of 0.84 at a cut off value of 12.75 ng/L, with sensitivity (76.9%) and specificity was 75.1%. The 30-day outcome of the patients admitted under cardiac speciality revealed no mortality in either group.An overall single cut-off value of 12.75 ng/L can be used in our population for ruling our ACS provided it is unaccompanied by other supportive clinical and ECG findings.

Background Our goals were to demonstrate receptor binding domain spike 1 (RBD S1) protein antibody (Ab) kinetic responses to multiple vaccines over approximately 180 days, neutralizing Ab effectiveness, and high-sensitivity cardiac troponin I (hs-cTnI) and T (hs-cTnT) responses in postvaccinated, non-SARS-CoV-2–infected subjects. Methods Blood specimens were collected pre- and postvaccinations from seronegative subjects. RDB S1 Abs were measured by the novel Qorvo Biotechnologies Omnia platform. Neutralizing Abs and hs-cTnI and hs-cTnT were measured on the ET Healthcare Pylon 3D. Results Two-dose vaccines (Pfizer, Moderna) had peak RBD S1 Ab concentrations about 45 to 55 days after both doses and showed declines over the next 50 to 70 days. The Janssen vaccine showed lower RBD S1 Ab peak concentrations, continued to increase over time, and plateaued after 60 days. There was strong neutralizing Ab response post vaccinations, with only 3 specimens, shortly before and shortly after vaccination, not showing a response. Specimens showed no hs-cTnI (all Conclusions We demonstrate in seronegative SARS-CoV-2 subjects that Pfizer and Moderna vaccinations provide strong, neutralizing RBD S1 Ab effectiveness, based on 2 different assays after 2 doses, with the Janssen single-dose vaccine showing a lower RBD S1 Ab response over 4 to 6 months. No myocardial injury was associated with the Pfizer postvaccination. The Qorvo Biotechnologies RBD S1 Ab assay measured on the Omnia platform has potential as a point-of-care platform.

Despite a growing body of literature on the physiological responses to ultramarathon, there is a paucity of data in females. This study assessed the female physiological response to ultramarathon and compared the frequency of perturbations to a group of race- and time-matched males.Data were collected from 53 contestants of an ultramarathon trail race at the Ultra-Trail du Mont-Blanc (UTMB®) in 2018/19. Before and within 2 h of the finish, participants underwent physiological assessments, including blood sampling for biomarkers (creatine kinase-MB isoenzyme [CK-MB], cardiac troponin I [cTnI], brain natriuretic peptide [BNP], and creatinine [Cr]), pulmonary function testing (spirometry, exhaled NO, diffusing capacities, and mouth pressures), and transthoracic ultrasound (lung comet tails, cardiac function). Data from eight female finishers (age = 36.6 ± 6.9 yr; finish time = 30:57 ± 11:36 h:min) were compared with a group of eight time-matched males (age = 40.3 ± 8.3 yr; finish time = 30:46 ± 10:32 h:min).Females exhibited significant pre- to postrace increases in BNP (25.8 ± 14.6 vs 140.9 ± 102.7 pg·mL -1 ; P = 0.007) and CK-MB (3.3 ± 2.4 vs 74.6 ± 49.6 IU·L -1 ; P = 0.005), whereas males exhibited significant pre- to postrace increases in BNP (26.6 ± 17.5 vs 96.4 ± 51.9 pg·mL -1 ; P = 0.002), CK-MB (7.2 ± 3.9 vs 108.8 ± 37.4 IU·L -1 ; P = 0.002), and Cr (1.06 ± 0.19 vs 1.23 ± 0.24 mg·dL -1 ; P = 0.028). Lung function declined in both groups, but males exhibited additional reductions in lung diffusing capacities (DL CO = 34.4 ± 5.7 vs 29.2 ± 6.9 mL⋅min -1 ⋅mm Hg -1 , P = 0.004; DL NO = 179.1 ± 26.2 vs 152.8 ± 33.4 mL⋅min -1 ⋅mm Hg -1 , P = 0.002) and pulmonary capillary blood volumes (77.4 ± 16.7 vs 57.3 ± 16.1 mL; P = 0.002). Males, but not females, exhibited evidence of mild postrace pulmonary edema. Pooled effect sizes for within-group pre- to postrace changes, for all variables, were generally larger in males versus females ( d = 0.86 vs 0.63).Ultramarathon negatively affects a range of physiological functions but generally evokes more frequent perturbations, with larger effect sizes, in males compared to females with similar race performances.

Background High-sensitivity cardiac troponin (hs-cTn) assays enable more precise use of traditional diagnostic strategies and earlier rule-out/rule-in at 0/1 h or 0/2 h after presentation of acute myocardial infarction (AMI). Availability of hs-cTn measurements at point-of-care (POC) can improve timely management of AMI patients. A roadmap for regulatory and analytical validation is exemplified with studies with the Atellica VTLi hs-cTnI at POC. Methods High-sensitivity performance was assessed with AACC/IFCC expert recommendations. Clinical Laboratory Standards Institute protocols were used for characterizing limit of blank, limit of detection (LoD), limit of quantitation (LoQ), 10% CV, precision, linearity, and analytic specificity with several reagent lots. Bland-Altman, Passing-Bablok, and hematocrit bias plots compared hs-cTnI measurement in lithium-heparin plasma (PL) and whole blood (WB) matrices. Results LoB was 0.55 ng/L; LoD and LoQ were 1.24 ng/L and 2.1 ng/Lm for PL and 1.60 ng/L and 3.7 ng/L for WB, respectively. The male 99th percentile is 27 ng/L, and female 99th percentile upper reference limit is 18 ng/L; 10% CVs were 6.7 ng/L for PL and 8.9 ng/L for WB. Also ≥50% of hs-cTnI values for healthy cohorts exceeded the LoD, confirming high-sensitivity performance. Linearity spanned from LoQ to 1250 ng/L. Specificity was >90% for 40 potential interferences; no hook effect was detected. WB and PL correlation was WB = 1.02*plasma + 0.3 ng/L (r = 0.996, n = 152). No hs-cTnI association with hematocrit was detected (R2 = 0.003). Conclusion This analytical roadmap showed high-sensitivity performance, good analytic characteristics, and excellent PL and WB agreement for the Atellica VTLi hs-cTnI POC system. Essential clinical performance studies in patients by intended POC users may now commence.

The relation of high-sensitivity cardiac troponin I (hs-cTnI) concentration and presence of obstructive coronary artery disease (CAD) in patients without myocardial infarction (MI) is unclear. Study participants selected from patients free of MI who underwent coronary angiography with or without intervention were enrolled, and hs-cTnI measured. A gradient boosting model was implemented to build a model for detection of CAD. Cox proportional hazard regression was used to assess the association of hs-cTnI and adverse cardiovascular (CV) outcome. Among 978 study participants, 607 patients (62%) had CAD. Higher concentrations of hs-cTnI were associated with chronic kidney disease, heart failure, CAD, male gender, current tobacco use, anemia, age, and low-density lipoprotein cholesterol. History of CAD, male gender, type 2 diabetes mellitus, hs-cTnI, anemia, age, and high-density lipoprotein cholesterol were the most influential factors for detection of CAD. The gradient boosting model had an area under the curve of 0.82, accuracy of 75%, sensitivity of 88%, specificity of 52%, positive predictive value of 76%, and negative predictive value of 72% for detection of CAD. Increase in 1 log unit of hs-cTnI was significantly associated with increased risk of incident MI (hazard ratio [HR] 1.34, 95% confidence interval [CI] 1.22 to 1.47, p0.001), CV mortality (HR 1. 24, 95% CI 1.11 to 1.39, p0.001), and composite of incident MI or CV mortality (HR 1.29, 95% CI 1.20 to 1.40, p0.001). In conclusion, among patients without acute MI and CAD, higher concentrations of hs-cTnI were associated with the presence of CAD and linked to increased risk of future CV events. ClinicalTrials.gov Identifier: NCT00842868.

W7 is a sarcomere inhibitor that decreases the calcium sensitivity of force development in cardiac muscle. W7 binds to the interface of the regulatory domain of cardiac troponin C (cNTnC) and the switch region of troponin I (cTnI), decreasing the binding of cTnI to cNTnC, presumably by electrostatic repulsion between the -NH

This study aimed to determine independent factors for developing postoperative hypertension using 4 biomarkers in patients receiving oral and maxillofacial surgery under general anesthesia. Brain natriuretic peptide (BNP), N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity myocardial troponin T (hs-TnT), and high-sensitivity myocardial troponin I (hs-TnI) were measured and preoperative echocardiograms were examined. Episodes of systolic blood pressure (SBP) ≥ 170 mmHg or diastolic blood pressure ≥ 100 mmHg within 1 week after surgery were considered postoperative hypertension. We analyzed 213 (130 men; 83 women) patients, who were divided into a postoperative hypertension group (HT group, n = 32) and a normal group (N group, n = 181). The HT group showed a higher LVMI (113.5 versus 100.1), higher E/e' of the lateral wall (9.1 versus 7.7), and higher BNP (39.2 versus 22.9 pg/mL), NT-proBNP (400.1 versus 143.9 pg/mL), and hs-TnT (15.6 versus 10.3 ng/L) concentrations compared to the N group. NT-proBNP and hs-TnT concentrations positively associated with E/e', but BNP and hs-TnI did not. NT-proBNP (AUC = 0.64, cutoff value: 117.0 pg/mL) and hs-TnT (AUC = 0.61, cutoff value: 11.0 ng/L) concentrations were effective for discriminating E/e' ≥ 12. Multivariate logistic regression analyses showed that risk factors responsible for developing postoperative hypertension were NT-proBNP and hs-TnT using biomarkers and E/e' as independent variables, and NT-proBNP and SBP at admission using biomarkers and SBP at admission as independent variables. These findings suggest that NT-proBNP and hs-TnT concentrations, and SBP at admission, are useful to predict postoperative hypertension after minor to moderate surgery, and that left ventricular filling pressure is a primary factor associated with postoperative hypertension.

Background: Arrhythmogenic cardiomyopathy (ACM) is an inherited genetic disorder of desmosomal dysfunction, and PKP2 (plakophilin-2) has been reported to be the most common disease-causing gene when mutation-positive. In the early concealed phase, the ACM heart is at high risk of sudden cardiac death before cardiac remodeling occurs because of mistargeted ion channels and altered Ca 2+ handling. However, the results of pathogenic PKP2 variants on myocyte contraction in ACM pathogenesis remain unknown. Methods: We studied the outcomes of a human truncating variant of PKP2 on myocyte contraction using a novel knock-in mouse model with insertion of thymidine in exon 5 of Pkp2 , which mimics a familial case of ACM (PKP2-L404fsX5). We used serial echocardiography, electrocardiography, blood pressure measurements, histology, cardiomyocyte contraction, intracellular calcium measurements, and gene and protein expression studies. Results: Serial echocardiography of Pkp2 heterozygous (Pkp2-Het) mice revealed progressive failure of the right ventricle (RV) in animals older than 3 months. By contrast, left ventricular function remained normal. ECGs of 6-month-old anesthetized Pkp2-Het mice showed normal baseline heart rates and QRS complexes. Cardiac responses to β-adrenergic agonist isoproterenol (2 mg/kg) plus caffeine (120 mg/kg) were also normal. However, adrenergic stimulation enhanced the susceptibility of Pkp2-Het hearts to tachyarrhythmia and sudden cardiac death. Histological staining showed no significant fibrosis or adipocyte infiltration in the RVs and left ventricles of 6- and 12-month-old Pkp2-Het hearts. Contractility assessment of isolated myocytes demonstrated progressively reduced Pkp2-Het RV cardiomyocyte function consistent with RV failure measured by echocardiography. However, aging Pkp2-Het and control RV myocytes loaded with intracellular Ca 2+ indicator Fura-2 showed comparable Ca 2+ transients. Western blotting of Pkp2-RV homogenates revealed a 40% decrease in actin, whereas actin immunoprecipitation followed by a 2,4-dinitrophenylhydrazine staining showed doubled oxidation level. This correlated with a 39% increase in troponin-I phosphorylation. In contrast, Pkp2-Het left ventricular myocytes had normal contraction, actin expression and oxidation, and troponin-I phosphorylation. Last, Western blotting of cardiac biopsies revealed that actin expression was 40% decreased in RVs of patients with end-stage ACM. Conclusions: During the early concealed phase of ACM, reduced actin expression drives loss of RV myocyte contraction, contributing to progressive RV dysfunction.

Percutaneous transluminal coronary angioplasty (PTCA) has been accepted as the elective treatment in many patients with coronary atherosclerotic obstruction. A slight increase in cardiac markers after the percutaneous coronary intervention (PCI) has been commonly reported. Some researchers have suggested that it predicts mortality and long-term complications. This study aimed to evaluate the occurrence of increased postoperative cardiac enzymes and determine the relationship between such an increase and clinical angiographic and technical variables. For this purpose, the descriptive study was performed in Hospital's cardiac ward from 2020-to 2021. One hundred twenty-two patients with stable coronary artery disease were studied for elective PTCA implanted with successful and uncomplicated stenting. Blood samples were taken from all patients to measure cardiac markers 20 hours after surgery. The normal range was CTnI ≤ 2ng/ml and CKMB ≤ 24 IU/L. Plasma levels of myocardial infarction and their relationship with clinical variables (including age, sex, risk factors for coronary artery disease, the severity of symptoms based on ccs class and previous history of acute coronary syndromes), angiographic including (lesion type, severity of stenosis) or related to the operation (operation on one or two vessels and direct stenting versus PTCA + stenting) were recorded in a questionnaire and observation sheets. The collected data were processed using descriptive statistics, frequency distribution tables, Chi-square, and student t-tests. Abnormal values of myocardial infarction were observed in 46.72% (57 patients). An increase in CTnI was observed in 39 patients (31.96%) and an increase in CKMB was seen in 31 patients (25.40%). Although the rise in CTnI exceeded the CKMB, the difference between the two was not statistically significant. The increased CTnI was significantly higher in older people, and the increase in CKMB was significantly higher in hypertensive individuals (p = 0.01). Based on the findings of this study, there is an increase in enzymes after successful and uncomplicated PCI selection. Increased CTnI occurs more frequently than CKMB. There is no relationship between enzyme enhancement and other clinical, angiographic, and technical variables.

Objectives To validate the analytical performance and diagnostic accuracy for non-ST-segment elevation myocardial infarction (NSTEMI) with a new high-sensitivity cardiac troponin I (hs-cTnI) assay on the automated light-initiated chemiluminescent assay (LiCA®) platform. Methods Comprehensive analytical validations were performed, and the 99th percentile upper reference limit (URL) from apparently healthy individuals were established. We evaluated the diagnostic performance of the assay for NSTEMI. Results The limit of quantitation (LoQ) were 1.9 ng/L (20% CV) and 5.1 ng/L (10% CV). The sex-specific 99th percentile URLs were 17.6 ng/L (4.2% CV) for men (age 20–79y) and 14.2 ng/L (4.9% CV) for women (age 19–89y) in serum, 14.4 ng/L (4.9% CV) for men (age 19–88y) and 12.9 ng/L (5.2% CV) for women (age 19–87y) in plasma, respectively. Detection rates in healthy individuals were from 98.7 to 99.1%. The correlation coefficient and median bias between LiCA and Architect were 0.985 and 0.1% (−2.0–2.9%) in full analytical range of serum specimens. In lower range ( Conclusions LiCA hs-cTnI is a precise, highly sensitive and specific assay that meets the requirement of a 3rd generation (level 4) high-sensitivity method. The diagnostic accuracy of LiCA assay for NSTEMI is comparable to the established Architect hs-cTnI assay.

At present, it remains unclear whether the effect on cryoinjury can be strongly exerted by contact of the balloon with the pulmonary vein (PV) ostium. The present study included 204 paroxysmal atrial fibrillation (PAF) patients who underwent an initial pulmonary vein isolation (PVI) using a cryoballoon from the Osaka Rosai Atrial Fibrillation ablation (ORAF) registry. The total balloon contact angle was measured from the equator line (sum of the angles of the upper side and bottom side in all PVs) under fluoroscopic imaging. The patients were stratified into three tertile groups according to the total balloon contact angle. We evaluated the relationship between the total balloon contact angle and clinical outcomes, including the value of acute myocardial injury marker (high-sensitive cardiac troponin I [hs-TnI]), arrhythmia recurrence, and PV reconnections in the repeated ablation. The total balloon contact angle was significantly associated with the hs-TnI value among the tertile groups (p 0.001) and a multiple regression analysis showed that the total balloon contact angle significantly correlated with the hs-TnI value (standardized beta-coefficient = 0.572, p 0.001). The balloon contact angle in PVs with PV reconnections was significantly lower than in those without (p = 0.044), while no significant differences in the recurrence of atrial fibrillation among the tertile groups were observed in the enrolled patients. The total balloon contact angle was significantly associated with the acute myocardial injury marker, hs-TnI. The total balloon contact angle was significantly associated with PV reconnections after cryoballoon ablation in patients who underwent a repeat ablation.

Magnolol is a component of the bark of Magnolia officinalis, which is a traditional herbal remedy used in China. In this study, we investigated whether magnolol can reduce myocardial injury induced by renal ischemia and reperfusion (I/R).Renal I/R was elicited by a 60-minute occlusion of the bilateral renal arteries and a 24-hour reperfusion in Sprague-Dawley rats. Magnolol was administered intravenously 10 minutes before renal I/R to evaluate its effects on myocardial injury induced by renal I/R.Renal I/R significantly increased the serum levels of creatine phosphokinase (CPK), lactate dehydrogenase (LDH), and cardiac troponin I and caused myocardial damage. The terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive nuclei and caspase-3 activation was significantly increased in the myocardium, indicating increase of apoptosis. Echocardiography revealed left ventricular dysfunction, as evidenced by reduction of left ventricular ejection fraction and left ventricular fractional shortening. Furthermore, serum levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 were significantly elevated, while the IL-10 level was suppressed. However, intravenously, pretreatment with magnolol at doses of 0.003 and 0.006 mg/kg 10 minutes before renal I/R significantly prevented the increases of CPK, LDH, and cardiac troponin I levels, as well as the histological damage and the apoptosis in the myocardium. Echocardiography showed significant improvement of left ventricular function. Furthermore, the increases in TNF-α, IL-1β, and IL-6 and the decrease in IL-10 were significantly limited, while Bcl-2 was increased and Bax was decreased in the myocardium. Phosphorylation of Akt and extracellular signal-regulated kinases 1 and 2 was increased, while phosphorylation of p38 and c-Jun N-terminal kinase was reduced.Magnolol reduces myocardial injury induced by renal I/R. The underlying mechanisms for this effect might be related to modulation of the production of pro- and anti-inflammatory cytokines and the limiting of apoptosis.

We established high-sensitivity cardiac troponin I (hsTnI) 99th percentile upper reference limits (URLs) for the Centaur XPT High-Sensitivity Troponin I assay (Centaur hsTnI; Siemens, Erlangen, Germany) and Atellica IM High-Sensitivity Troponin I assay (Atellica hsTnI; Siemens) and assessed the effect of outlier elimination.The reference population comprised 380 men and 387 women, satisfying the strict systematic reference population criteria. After reference population verification by the N-terminal pro-B-type natriuretic peptide (NT-proBNP) assay, 99th percentile URLs for Centaur hsTnI and Atellica hsTnI were calculated before and after outlier elimination.The 99th percentile URL for Centaur hsTnI was 60.4 (men, 74.7; women, 57.5) ng/L and that for Atellica hsTnI was 59.6 (men, 75.2; women, 55.1) ng/L. After the elimination of 61 (8.0%) outlier samples in Centaur hsTnI and 58 (7.6%) in Atellica hsTnI, the 99th percentile URLs were 13.5 ng/L (men, 15.3 ng/L; women, 11.9 ng/L) and 13.4 ng/L (men, 15.5 ng/L; women, 12.9 ng/L), respectively, significantly lower than those before outlier elimination. The CVs at the 99th percentile URLs were 5.2% and 3.5%, respectively. The measurable fractions among the reference population were 91.5% and 93.4%, respectively. Performance evaluation of Atellica B-type natriuretic peptide (BNP), Atellica NT-proBNP, Centaur hsTnI, and Atellica hsTnI showed outstanding results.The Korean hsTnI 99th percentile URLs calculated in this study were significantly lower after outlier elimination than before. Centaur hsTnI and Atellica hsTnI meet the "Guideline acceptable" and "Level 3 (second generation, high sensitivity)" requirements, satisfying international standards.

Introduction:The European Society of Cardiology (ESC) 2020 guidelines propose an algorithm for in-hospital management of non-ST-elevation myocardial infarction (NSTEMI) based on risk stratification according to clinical, electrocardiographic, and biological data. However, out-of-hospital management is not codified.Study Objective:The objective of the present study was to evaluate the role of high-sensitivity cardiac troponin-I in out-of-hospital management of NSTEMI by Emergency Medical Services (EMS).Methods:This monocentric, retrospective, observational study analyzed the files of all patients having received a troponin assay in the EMS of Beaujon University Hospital, AP-HP (Paris region, France) from January 1, 2020 through December 31, 2020. Patients were classified as low risk, high risk, or very high risk according to the ESC 2020 algorithm at the time of their hospital treatment. The relationship between troponin in point-of-care and risk level according to time to onset of pain was analyzed using logistic regression. A search for predictors of risk level was performed using multivariate analysis. A P value Results:Out of 309 patients in the file, 233 were included. Men were 61% and the median age was 63 years. A positive troponin assay was associated with high-risk or very high-risk stratification regardless of the time to onset of pain (P Conclusion:The use of point-of-care troponin in EMS, combined with clinical and electrical criteria, allows risk stratification of NSTEMI patients from the prehospital management stage and optimization of referral to an appropriate care pathway. Patients classified as low risk should be referred to the emergency department (ED) and patients classified as high risk or very high risk to the cardiac intensive care unit or percutaneous coronary intervention (PCI) center.

A recent study showed higher high-sensitivity cardiac troponin I (hs-cTnI) concentrations in healthy dogs eating grain-free (GF) compared to those eating grain-inclusive (GI) diets.Healthy dogs with subclinical cardiac abnormalities eating GF diets at baseline will show improvements in cardiac biomarkers and echocardiographic variables after diet change, whereas healthy dogs eating GI diets at baseline will not improve.Twenty healthy dogs with subclinical cardiac abnormalities (12 Golden Retrievers, 5 Doberman Pinschers, 3 Miniature Schnauzers).This prospective study included dogs with increased hs-cTnI or N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentrations, or echocardiographic abnormalities. Mixed modeling was used to evaluate echocardiographic, hs-cTnI, and NT-proBNP differences between groups (GF or GI diet at baseline) over time (1 y after diet change).Ten GF and 10 GI dogs were evaluated. There were statistically significant time: group interactions for hs-cTnI (P = .02) and normalized left ventricular internal systolic diameter (LVIDsN; P = .02), with GF dogs showing larger decreases in these variables than GI dogs. Median (range) hs-cTnI (ng/mL) for GF dogs was 0.141 (0.012-0.224) at baseline and 0.092 (0.044-0.137) at 1 y, and for GI dogs was 0.051 (0.016-0.195) at baseline and 0.060 (0.022-0.280) at 1 y. Median LVIDsN for GF dogs was 1.01 (0.70-1.30) at baseline and 0.87 (0.79-1.24) at 1 y, and for GI dogs was 1.05 (0.84-1.21) at baseline and 1.10 (0.85-1.28) at 1 y.Decreased hs-cTnI and LVIDsN in GF dogs after diet change supports reversibility of these subclinical myocardial abnormalities.

Dilated cardiomyopathy (DCM) is the most common cardiac disease in large breed dogs. The disease can start with arrhythmias or with systolic dysfunction of the myocardium.To describe screening methods for DCM in various breeds and provide a new, modified staging system.Screening for occult DCM should start at three years of age and use Holter monitoring in Boxers and Dobermans and might be useful also in other breeds. Single ventricular premature complexes (VPCs) can be detected in many healthy dogs, but healthy animals typically have50 VPCs in 24 h and demonstrate minimal complexity most often occurring only as single ectopic beats. In general,100 VPCs in 24 h was recommended as the cut-off value for establishing a diagnosis of DCM. However, there are breed-specific recommendations related to Holter recording diagnosis of DCM in Dobermans and Boxers. Yearly screening over the life of a dog is recommended, as a one-time screening is not sufficient to rule out the future development of DCM. Several echocardiographic methods such as M-mode derived measurements, the measurement of the left ventricular (LV) volume by Simpson's method of discs (SMOD), and E-point to septal separation (EPSS) are recommended for screening purposes. The value of additional tests such as cardiac biomarkers (troponin I and N-terminal pro-B-type natriuretic peptide) as well as a 5-min resting electrocardiogram (ECG) or newer echocardiographic methods such as strain measurements is discussed.This review suggests some guidelines for screening for DCM in various breeds.

Chest pain is a common clinical complaint for which myocardial injury is the primary concern and is associated with significant morbidity and mortality. To aid providers’ decision-making, we aimed to analyze the electrocardiogram (ECG) using a deep convolutional neural network (CNN) to predict serum troponin I (TnI) from ECGs. We developed a CNN using 64,728 ECGs from 32,479 patients who underwent ECG within 2 h prior to a serum TnI laboratory result at the University of California, San Francisco (UCSF). In our primary analysis, we classified patients into groups of TnI

Objective: Our aim is to determine the levels of troponin-I and some coagulation markers (D-dimer, fibrinogen and International Normalized Ratio (INR)) in coronavirus disease 2019 (COVID-19) patients and to investigate the effects of these markers on mortality. Patients and Methods: It is planned as a descriptive, cross-sectional and analytical study. The study was conducted by retrospectively scanning the files of COVID-19 patients who applied to Inonu University Turgut Ozal Medical Center between 01.03.2020 and 31.12.2020. Levels of cardiac troponin I markers and coagulation parameters (D-dimer, fibrinogen and INR) were detected. Results: The results of a total of 1858 patients were obtained. One thousand, three hundred and twenty-six patients with only troponin I and D-dimer results (Group 1), 606 patients with only troponin I and fibrinogen results (Group 2), and 1308 patients with only troponin I and INR results (Group 3) were included. Troponin I levels were significantly higher in all patients who died. 96.6% of the patients with high D-dimer levels died in Group 1, 85.5% of the patients with high fibrinogen levels died in Group 2 and 77.3 % of the patients with high INR levels died in Group 3. Conclusion: Measurements of troponin-I and coagulation markers such as D-dimer, fibrinogen and INR can help predict clinical severity and mortality in COVID-19 patients.

Hypertrophic cardiomyopathy is an inherited disorder due to mutations in contractile proteins that results in a stiff, hypercontractile myocardium. To understand the role of cardiac stiffness in disease progression, here we create an in vitro model of hypertrophic cardiomyopathy utilizing hydrogel technology. Culturing wild-type cardiac myocytes on hydrogels with a Young’s Moduli (stiffness) mimicking hypertrophic cardiomyopathy myocardium is sufficient to induce a hypermetabolic mitochondrial state versus myocytes plated on hydrogels simulating healthy myocardium. Significantly, these data mirror that of myocytes isolated from a murine model of human hypertrophic cardiomyopathy (cTnI-G203S). Conversely, cTnI-G203S myocyte mitochondrial function is completely restored when plated on hydrogels mimicking healthy myocardium. We identify a mechanosensing feedback mechanism between the extracellular matrix and cytoskeletal network that regulates mitochondrial function under healthy conditions, but participates in the progression of hypertrophic cardiomyopathy pathophysiology resulting from sarcomeric gene mutations. Importantly, we pinpoint key ‘linker’ sites in this schema that may represent potential therapeutic targets.

Cardiac troponins are highly sensitive and specific biomarkers for cardiac injury. Previous studies evaluating the effect of positive airway pressure (PAP) on cardiac troponins in patients with sleep-disordered breathing (SDB) have yielded conflicting results. The meta-analysis was performed to examine the effect of PAP on cardiac troponins in SDB patients.PubMed, Web of Science, and EMBASE before September 2021 on original English language studies were searched. The data on cardiac troponins in both baseline and post-PAP treatment were extracted from all studies. The data on the change of cardiac troponins in both PAP and control group were extracted from randomized controlled trials. Standardized mean difference (SMD) was used to synthesize quantitative results.A total of 11 studies were included. PAP treatment was not associated with a significant change in cardiac troponin T between the baseline and post-PAP treatment (SMD = -0.163, 95% confidence interval [CI] = -0.652 to 0.326, z = 0.65, p = .514). The pooled estimate of SMD of cardiac troponin I between the pre- and post-PAP treatment was 0.287, and the 95% CI was -0.586 to 1.160 (z = 0.64, p = .519). The pooled SMD of change of cardiac troponin T between the PAP group and control group was -0.473 (95% CI = -1.198 to 0.252, z = 1.28, p = .201).This meta-analysis revealed that PAP treatment was not associated with any change of cardiac troponin in SDB patients.